Blond S, Mertens P, David R, Roulaud M, Rigoard P
Department of Neurosurgery, Lille University Hospital, 59037 Lille Cedex, France.
Department of Neurosurgery, Lyon University Hospital, 69677 Lyon Cedex, France; Laboratory of Anatomy, Faculty of Medicine, 69677 Lyon Cedex, France.
Neurochirurgie. 2015 Mar;61 Suppl 1:S45-56. doi: 10.1016/j.neuchi.2014.11.001. Epub 2015 Jan 14.
Beyond initial lesions, any form of spinal (re)operation can cause direct potential aggression to the nervous system by contact with neural tissue or by imprinting a morphological change on the neural tissue. The potential consequences of nerve root injury affect both peripheral and axial dermatomal distribution. The hypothesis of a possible neuropathic aspect associated with the back pain component of failed back surgery syndrome (FBSS) therefore appears to be reasonable. Its pathophysiology remains unclear due to the permanent interplay between nociceptive and neuropathic pain components, resulting in the coexistence of physiological and pathological pain at the same anatomical site. This paper is designed to extensively review the fundamental mechanisms leading to chronification of pain and to suggest considering the emerging concept of "neuropathic back pain".
Literature searches included an exhaustive review of 643 references and 74 book chapters updated by searching the major electronic databases from 1930 to August 2013.
Inflammatory and neuropathic back pain could be distinguished from pure nociceptive pain as a result of an increased activity and responsiveness of sensitized receptors at the peripheral nervous system and also as a consequence of increased afferent inflow to the central nervous system, moving to a new, more excitable "wind-up" state. This can be clinically translated to an amplified response to a moderate/intense stimulus (primary hyperalgesia) or an aversive sensation provoked by the activation of low-threshold mechanoreceptors through non-noxious stimuli, which defines allodynia. Activated non-neuronal cells including microglia have been found to be cellular intermediaries in mechanical allodynia. Major changes in the spinal cord are the loss of inhibitory mechanisms, resulting in an increased activity of interneurons or projection neurons and a structural reorganization of the central projection pattern. This abnormal excitability of sensory neurons is coupled to changes in the neurotransmitter phenotype, which could induce a resistance to conventional analgesic treatments.
A clear understanding of the factors leading to the chronification of back pain should help us to move to the choice of mechanism related pain treatments to improve outcomes in FBSS chronic condition.
除了初始损伤外，任何形式的脊柱（再）手术都可能通过与神经组织接触或在神经组织上留下形态学改变而对神经系统造成直接潜在侵害。神经根损伤的潜在后果会影响外周和轴向皮节分布。因此，与失败的脊柱手术综合征（FBSS）的背痛成分相关的可能存在神经病变方面的假设似乎是合理的。由于伤害性疼痛和神经病理性疼痛成分之间的持续相互作用，其病理生理学仍不清楚，导致生理和病理性疼痛在同一解剖部位共存。本文旨在广泛回顾导致疼痛慢性化的基本机制，并建议考虑新兴的“神经病理性背痛”概念。
文献检索包括对643篇参考文献和74章书籍进行详尽回顾，通过检索1930年至2013年8月的主要电子数据库进行更新。
炎症性和神经病理性背痛可与单纯伤害性疼痛区分开来，这是由于外周神经系统中致敏受体的活性和反应性增加，以及传入中枢神经系统的传入流量增加，从而进入一种新的、更易兴奋的“wind-up”状态。这在临床上可转化为对中度/强烈刺激的放大反应（原发性痛觉过敏）或通过非伤害性刺激激活低阈值机械感受器所引发的厌恶感，即定义为异常性疼痛。已发现包括小胶质细胞在内的活化非神经元细胞是机械性异常性疼痛的细胞中介。脊髓的主要变化是抑制机制丧失，导致中间神经元或投射神经元活性增加以及中枢投射模式的结构重组。感觉神经元的这种异常兴奋性与神经递质表型的变化相关联，这可能导致对传统镇痛治疗产生抗性。
清楚了解导致背痛慢性化的因素应有助于我们转向基于机制的疼痛治疗选择，以改善FBSS慢性病的治疗效果。
